| Sustained
Response to Interferon-based Therapy Reduces Risk of Diabetes in Hepatitis C Patients By
Liz Highleyman Several
studies have shown that people with chronic hepatitis C have an increased risk
of developing insulin resistance and diabetes mellitus, but it is not clear whether
this excess risk can be reduced with interferon-based
therapy. As
reported in the March 2009 issue of Hepatology, Japanese researchers retrospectively
analyzed the incidence of and predictive factors for type 2 (also known as adult-onset)
diabetes in 2842 hepatitis C patients who did not have diabetes at baseline and
who were treated with conventional interferon, either as monotherapy (n = 2417)
or in combination with ribavirin (n = 425).
Over a mean follow-up period
of 6.4 years, overnight (12-hour) fasting blood samples or casual blood samples
were regularly collected to test for development of diabetes.
Results
36.7% of patients who received interferon
monotherapy and 68.0% of those treated with interferon
plus ribavirin achieved sustained virological
response (SVR).
143 of the 2842 participants (5.0%) developed type 2 diabetes during follow-up.
Cumulative diabetes incidence rates were 3.6% at 5 years, 8.0% at 10 years, and
17.0% at 15 years.
In a multivariate analysis, diabetes incidence after completion of antiviral therapy
was significantly associated with:
Advanced liver fibrosis (hazard
ratio [HR] 3.3; P < 0.001);
Lack of sustained virological response (HR 2.7; P < 0.001);
Presence of "pre-diabetes," or elevated blood glucose, at baseline (HR
2.2; P < 0.001);
Age > 50 years (HR 2.1; P < 0.001).
In
conclusion, the study authors wrote, "Our results indicate sustained virological
response causes a two-thirds reduction in the risk of type 2 diabetes development
in HCV positive patients treated with interferon."
Department of
Hepatology, Toranomon Hospital, Tokyo, Japan
4/21/09
Reference Y
Arase, F Suzuki, Y Suzuki, and others. Sustained virological response reduces
incidence of onset of type 2 diabetes in chronic hepatitis C. Hepatology
49(3): 739-744. March 2009. (Abstract).
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